الفهرس | Only 14 pages are availabe for public view |
Abstract Acute kidney injury (AKI) is a protean syndrome of varied severity. It is characterized by a rapid decline in the glomerular filtration rate (GFR) and retention of nitrogenous waste products such as blood urea nitrogen (BUN) and creatinine. AKI is diagnosed using blood urea, and serum creatinine levels, but serum creatinine is an unreliable indicator of kidney function during acute changes, as serum creatinine level can vary widely with age, gender, muscle mass, muscle metabolism, medications, and hydration status, another cause is that its concentration may not change until about 50% of kidney function has already been lost, at lower rates of glomerular filtration the amount of tubular secretion of creatinine results in overestimation of renal function, during acute changes in renal filtration, serum creatinine does not accurately depict kidney function until steady state equilibrium has been reached, which may require several days. The application of innovative technologies such as functional genomics and proteomics to human and animal models of AKI had uncovered several novel biomarkers, such as; neutrophil gelatinase associated lipocalin (NGAL) which can be measured in blood and urine and was found to diagnose AKI 1-3days before serum creatinine is elevated. Urinary interleukin 18 (IL-18) was found to detect contrast induced nephropathy 24 hours before serum creatinine elevation. Kidney injury molecule 1 (KIM-1) level in renal transplant patients was found to correlate with the incidence of graft loss. Growth related oncogene alpha (GRO-α) was found to be elevated in renal transplant patients whose renal biopsy showed acute tubular necrosis. Alpha-1 microglobulin was found to predict the need for renal replacement therapy in non-oliguric acute renal failure. Key words: AKI, biomarkers, NGAL, IL-18, KIM-1, GRO-α, Alpha-1 microglobulin,, cystatin C, Fetuin-A, Meprin. |